The Psychologisation
of Illness

Ellen Goudsmit

Introduction

Psychologisation
describes the emphasis on psychological factors where there is little or no
evidence to justify it (1). It's a process where relevant findings are ignored
or downplayed in favour of data from incomplete examinations, flawed research or
anecdotal reports. In a clinical context, differential diagnoses may be
dismissed prematurely while psychological explanations are readily accepted.
Psychologisation does not refer to situations where there is sound evidence that
psychological factors play a significant role, or where all the arguments are
discussed and the psychological explanations are deemed the most persuasive.

Psychologisation
is a serious issue because it leads to misdiagnosis, inappropriate treatment and
unnecessary psychological distress (2). Moreover, it undermines the general
population's confidence in orthodox medicine and reduces their trust in its
practitioners. Yet, despite the dangers, psychologisation has received little
attention in medical texts. In this article, I will discuss the main reasons
underlying psychologisation and examine whether it has influenced views about
food allergies and intolerance.

Psychologisation
in clinical practice.

Many
cases of psychologisation in clinical practice occur because doctors jump to
conclusions without checking that their psychological explanations are correct.
For instance, Treasure et al (3) described how three women suffering from
"breathlessness and panic symptoms" were admitted to their accident
and emergency department. The initial diagnosis was hysterical hyperventilation,
as a result of which two of the patients were referred to a psychiatrist while
the third was discharged with a prescription for diazepam. Within three days
however, the women returned and tests revealed that they were suffering from
diabetes. According to Treasure et al, the assumption that the problem was
psychological had led "to the dangerous omission of physical examination,
basic nursing observations, and urine analysis. In all these patients a simple
test for glycosuria would have made the diagnosis obvious and the consequent and
considerable risk to the patients could have been avoided."

Another
typical example is that of a woman who developed anxiety, fatigue and
intermittent cramp-like abdominal pains after changing her job. Her GP diagnosed
irritable bowel syndrome (IBS), precipitated by the stress at work, and advised
a short period of sick leave. As the pain did not subside, she continued to
consult her GP but neither he, nor the other doctors who saw her, questioned the
diagnosis. A few months later, she noticed that the pain was associated with
"spasms visible through the abdominal wall", but the doctors who
examined her at the local casualty department continued to blame IBS. When the
patient consulted the author of the report, she found "an easily palpable
mass in the left iliac fossa" and an emergency operation confirmed cancer
of the sigmoid colon. As in the case above, doctors had overlooked organic
disease and wrongly attributed all the symptoms to a psychological cause.

Psychologisation
in the literature on aetiology.

Some
of the most interesting examples of psychologisation can be found in the
theoretical discussions of disease. For instance, Booth (5) offered a
psychodynamic view of tonsillitis, arguing that many cases represented a love
relationship with a bacteria in which the patient establishes "libidinous
contact on the earlier oral instead of the later genital level... the object of
the oral strivings is no longer another human being, but bacteria... Such
substitutions of bacteria for a human being makes biologic sense considering the
fact that the basic object of the sex act is the copulation of the sex cells:
primitive unicellular organisms like bacteria."

This
is a typical case of psychologisation, not only because of the poor quality of
the supportive evidence but also because the author ignored all the relevant
data to the contrary. For more recent examples of speculative and over
simplistic hypotheses, see Hay and Millenson (6, 7).

Most
cases of psychologisation are not as extreme and indeed, may not be recognised
except by colleagues who are familiar with the research. Perhaps the best
examples of the more subtle forms of psychologisation can be found in the
British medical literature on myalgic encephalomyelitis (ME) and chronic fatigue
syndrome (CFS)1. Many articles on
these conditions feature highly selective discussions of the scientific data,
with an emphasis on findings relating to psychiatric morbidity and a tendency to
ignore or dismiss evidence of disease (8).

The
problems began in 1970, with the publication of a paper on the epidemic, which
closed the Royal Free Hospital during the summer of 1955. 'Royal Free disease'
resembled a viral infection and affected over 200 members of staff, the majority
of whom were female. It was eventually reclassified as ME but one of the
consultants involved in their treatment noted later that he and his colleagues
had considered the possibility of hysteria. However, "the occurrence of
fever in 89%, of lymphadenopathy in 79%, of ocular palsy in 43% and of facial
palsy in 19% rendered it quite untenable"(9).

Fifteen
years after the event, psychiatrists McEvedy and Beard were given access to some
of the incomplete reports as well as the notes of those who were not
thought to have had 'Royal Free disease' (10). However, instead of restricting
their conclusions to the sample studied, they dismissed the whole outbreak as a
case of mass hysteria.

They
based their view on three main arguments. Firstly, they claimed that most of
those affected had been young and socially segregated young females. Secondly,
they argued that the illness had not spread beyond the institutional population.
Thirdly, they alleged that it had not affected a significant number of men.
Notable omissions in their account included what might have triggered the
anxiety among the older and more experienced health professionals involved, or
what may have led to the lymphadenopathy or the morphological abnormalities seen
in circulating lymphocytes (11, 12).

In
fact, there are many arguments against the mass hysteria theory (9, 13, 14),
although these are generally ignored (e.g. 15, 16). For example, the nurses were
not socially segregated as suggested by McEvedy and Beard (17) and in terms of
age, the illness was more common amongst those over forty (11). As for the
predominance of females, this was true only in relation to the non-resident
staff. The attack rates for resident men and women were 19 and 20 per 100
respectively (11).

It
has also been pointed out that if the epidemic had resulted from anxiety in a
segregated group of women, then one would have expected a higher proportion of
cases in the Elizabeth Garrett Anderson Hospital and Maternity Home (18). These
institutions were part of the Royal Free Hospital group and were run for and
staffed entirely by women. However, less than 7% of the patients came from these
units - and only the Eastman Dental Hospital recorded fewer cases (11).

Another
argument against McEvedy and Beard's explanation is that some of the features of
the outbreak were simply not typical of mass hysteria. According to Sirois (19),
most of these episodes last between 10 and 20 days and primarily affect
adolescent women. In contrast, the outbreak at the Royal Free Hospital lasted
for four months (from July 13th 1955 until November 24th) and only a minority of
those affected were younger than 20 (11).

Finally,
the literature on sporadic cases, which clearly resembled those seen in the
epidemic, proved that the outbreak not only spread beyond the institutional
population (20, 21, 22) but also beyond London (9). Moreover, there was evidence
of viral involvement both in the Royal Free patients (Parish 1994, personal
communication) and in people with an identical disorder examined later (22). On
the basis of these findings alone, the suggestion that all the cases at the
Royal Free were the result of mass hysteria is unsustainable.

In
the light of the available evidence, McEvedy and Beard's article should have
been dismissed as deeply flawed and biased. Instead, it was widely accepted and
became highly influential. For many years, their conclusions diverted the
scientific community's attention away from the virological and neurological
aspects of the disease and thus limited the research, and our understanding of
ME. More importantly, their dualistic 'mind or body' approach provided the basis
for the organic versus psychological debate, which has dominated the literature
on the illness for the past two decades (15, 23, 24).

The
causes of psychologisation

1.
Stereotypical views of women

Although
the literature shows that men are not immune, most of the reports relating to
psychologisation feature women. In older texts, female patients were often
portrayed as suggestible, emotionally unbalanced, irrational, manipulative and
unable to cope with relatively minor 'stress'. For instance, authors writing
about dysmenorrhoea claimed it was more common in "highly strung",
"nervous" or "neurotic" women, and speculated how a 'faulty
outlook' might lead to "an exaggeration of minor discomfort"
(25).

Premenstrual
syndrome was also regarded as a mild and benign problem which women should be
able to endure without medical intervention. As in the accounts of
dysmenorrhoea, authors often implied a link with somatisation, with suggestions
that certain women were guilty of exaggerating their distress, perhaps to escape
responsibility or effort (26). Conversely, most of these articles did not
consider the effect of recurring symptoms on the women's self-confidence and
self-esteem, or the possibility that this could explain the raised scores on
psychometric tests (27). Ignoring virtually all arguments to the contrary, many
authors regarded emotional problems as the cause, rather than the result of
ongoing ill-health (25).

A
more specific illustration of the influence of gender stereotypes was reported
by Roberts (28). She related the story of a brother and sister, both of whom
suffered from migraines (28). When the doctor was asked about his thoughts on
the woman, he attributed her headaches to her social situation - tensions and
problems caused by the fact that she was not married, did not have children, and
that she was a 'career woman'. In contrast, he regarded her twin brother's
migraines as having a genetic and biochemical basis and refused to consider a
social explanation.

One
reason why some doctors may be more inclined to psychologise the illnesses
reported by women is the way in which many express their distress.
Discussing her experiences as a physician, Gillespie (29) suggested that:
"men tend to speak from fact, women tend to speak from emotion." Thus,
women may refer to pain in terms of ruining their marriage and destroying their
life. They relate the effects of their symptoms rather than their nature.
According to Gillespie, this emphasis on the mental anguish can mislead some
doctors into assuming a psychological aetiology.

A
similar phenomenon has been documented in relation to ethnic groups. In one
study, Zola (30) found that Italian Americans were given more psychiatric
diagnoses than patients with an Anglo-Saxon or Irish background. Accounting for
the findings, Zola noted that Italians had a tendency to report the effects of
their symptoms and he suggested that their behaviour could have been interpreted
as "overacting". As in the case of women, the way in which these
patients described their symptoms might have influenced the clinicians to focus
on one explanation and to dismiss another.

Some
of the stereotypical ideas about female patients may have originated during
medical training. As one female student told Howell (31): "women's
illnesses are assumed psychosomatic until proven otherwise." Another
observed that women are often "portrayed as hysterical or as nagging
mothers or as having trivial complaints. Men are almost never pointed to as
having a psychological component to their illnesses - this is generally
attributed to women."Howell
also reported that mothers were sometimes described as "complaining",
and that older women were deemed to be "demanding and bitchy".

The
belief that psychological factors play a major role in the conditions reported
by women may be one reason why they are often investigated less thoroughly than
the same symptoms in men. For example, a small study by Armitage et al (32)
revealed that physicians ordered more extensive tests and procedures for men
than for women with the same complaint.Discussing
the findings, the authors suggested that the physicians "might have been
responding to current stereotypes that regard the male as typically stoic and
the female as typically hypochondriacal".

Such
a view is supported by Ayanian and Epstein (33) who studied patients
hospitalised for coronary heart disease and found that the women underwent fewer
diagnostic and therapeutic procedures than the men. Likewise, Steingart et al
reported that women with cardiac disease were offered fewer procedures like
coronary by-pass surgery than men, even though the women were more disabled and
those procedures could have significantly lessened the symptoms (34). The
authors stated that the symptoms of chest pain in women were more likely to be
attributed to non-cardiac causes but they did not speculate which. In a more
recent study, Pope et al (35) assessed patients with acute cardiac ischemia who
were mistakenly discharged from the emergency departments of ten American
hospitals. They found that discharge was more likely if the patient was a woman
aged 55 years or younger, 'non-white', or if the principal symptom was shortness
of breath. Although this study does not illustrate overt psychologisation, it
shows that in this age of evidence-based medicine, variables like gender, age
and race continue to influence some doctors' clinical judgement.

Despite
the large number of reports detailing apparent 'sex-discrimination', the extent
of gender bias in medicine is difficult to assess. For instance, several
analogue studies found no significant differences in the percentage of men and
women who were given a psychogenic diagnosis or psychotropic drugs (36).
However, it is probably fair to say that stereotypical attitudes still play a
role in many cases of psychologisation, though to varying degrees and alongside
other variables such as ethnic background and age.

2.
Lack of clarity relating to symptoms.

Another
important factor underlying many cases of psychologisation is the difficulty in
diagnosing certain conditions. For instance, Himmelhoch et al (37) described
eight patients with subacute encephalitis, of whom seven were initially
diagnosed as having functional psychiatric disorders. They concluded that:
"the bizarre behaviour induced physicians to ignore neurological findings,
to overlook evidence of organic syndromes (such as intermittent lucidity and
markedly abnormal electroencephalograms) and to make functional diagnoses."

Likewise,
Randy Shilts noted in his history of the AIDS epidemic that: "doctors
frequently missed the damage to the central nervous system, writing off the
often vague symptoms of dementia as related to stress or depression" (38).
Similarly, the predominance of non-specific symptoms like weakness and fatigue
have been blamed for the failure to correctly diagnose cases of myasthenia
gravis (39).

3.
Lack of evidence.

The
lack of clarity in relation to symptoms is not the only factor which can
complicate the diagnostic process. There are now so many laboratory tests
available, that some doctors may interpret 'absence of evidence' as 'evidence of
absence' (40). Thus if tests fail to identify a physical cause, some may reason
that there is no physical cause to be identified and that the symptoms therefore
have a non-organic, i.e. psychological cause. Consequently, patients may be told
that "there is nothing wrong" or that the illness "is all in your
head"; two assessments which not only contradict actual experience but
which also imply that the distress is not legitimate. Where this occurs, the
physician's failure to define the illness as a 'disease state' is often an
additional source of suffering which can undermine the patient's psychological
health. As Stewart and Sullivan (41) observed, the emotional conflicts and
tension caused by the 'misdiagnosis' of pathology can lead to "a type of
iatrogenic disease" characterised by symptoms such as "feelings of
frustration, worry and intermittent periods of depression."

One
person to have experienced this type of psychologisation is the late Jacqueline
Du Pré. In her biography of the cellist, Carol Easton (42) wrote:

"There
is no specific test for multiple sclerosis.Its early symptoms - fatigue, loss of sensation, weakness and visual
changes - are frequently misdiagnosed as psychoneurosis or an even more severe
psychiatric disorder, such as hysteria, particularly in women. When doctors
could find no organic cause for her complaints, they prescribed a year's rest,
and referred her to a psychiatrist... When she consulted a doctor in Australia
about her tenacious fatigue and occasional double vision in her right eye, he
dismissed her symptoms as "adolescent trauma" and suggested she take
up a relaxing hobby."

According
to the Multiple Sclerosis Society (personal communication), such an experience
is not rare and after months or years of having been told their symptoms are
psychological or psychosomatic, many patients feel relieved when they learn that
they have MS. Robinson (43) confirmed this in his study, stating that: "the
disclosure of the diagnosis gave back to many respondents their credibility and
legitimised their strange behaviours which had previously been labelled as
neurotic, hypochondria, malingering or drunk."

Further
evidence that diagnostic uncertainty can influence attitudes towards patients
comes from a study conducted among nurses (44). They were asked to rate the
degree of suffering, the need for pain relief and the personality of patients
with severe pain. One of the vignettes they were given listed signs of objective
pathology, the other did not. The results showed that the nurses attributed less
intense pain when the patient in the vignette had no signs of pathology or when
the condition was chronic. Moreover, ratings of the patient's personality were
significantly more positive when pathology was present than when it was
negative. According to the researchers, the nurses relied on the biomedical
model of pain which suggests that this symptom is a physical response to tissue
damage. The failure to find evidence of tissue injury led to a psychogenic
labelling, as did chronicity, the suggestion being that after a time patients
should have adapted to their pain.

4.Cause or effect?

Some
cases of psychologisation may be due to the reversal of cause and effect. For
instance, in their review of articles on severe dysmenorrhoea, Lennane and
Lennane (25) found that doctors tended to view their patients' fear and dislike
of menstruation as a cause of their pain, rather than as a result. Similarly,
the frustration and irritability documented in women with mastalgia were for
many years dismissed as an expression of psychoneurosis, rather than the effects
of recurrent pain. However, when researchers studied these women, they were
found to be "no more neurotic" than people with varicose veins (45).
It is now generally accepted that most cases of mastalgia are related to
hormonal imbalance (Brush, personal communication).

The
tendency to view psychological states and traits as a cause rather than the
result of illness might also explain some of the psychological explanations for
Parkinson's Disease (46) premenstrual syndrome (27), cancer (47), multiple
sclerosis (48, 49) and the diabetes personality (50).

5.Interpretation of research findings.

When
research reveals an apparent association between illness on the one hand and
psychological symptoms, states and traits on the other, it is often difficult to
determine the direction of the relationship. In addition to the possibility that
the psychological variable caused the disease, there are a number of other
explanations which should be considered (51). They include:

a.
Coincidence. The likelihood that both the illness and the psychological
variable may have been caused by independent agents and that they are not
related.

b.
The presence of an external agent.A
third variable, for instance, environmental pollution, might have caused both
phenomena.

c.
The existence of an internal agent. For example, heredity or an immunological
or neurological dysfunction may have influenced both psychological and
physical variables.

d.
The influence of a behavioural agent. Certain behaviours may have induced
emotional states and affected the person's health. For instance, eating a poor
diet could result in depressed mood as well as disease.

e.
The presence of an intervening agent. Here an event or state intervenes
between the psychological and biological factors, causing them to correlate.
For example, depression caused by bereavement may compromise immune function
which then increases one's predisposition to or exacerbates ill-health.

f.
Disease causation. A sixth possibility is that a disease caused a particular
psychological reaction. Since it is often difficult to pinpoint the actual
onset of a disease, it is possible that certain physiological changes preceded
the psychological ones. Thus depression may be the first symptom of pancreatic
cancer, multiple sclerosis or Parkinson's disease (52).

The
interpretation of an apparent link between illness and psychological variables
is further complicated by methodological problems, notably the use of different
diagnostic criteria and measures. This has resulted in an astonishing range of
prevalence figures for psychiatric morbidity in people with cancer, diabetes,
multiple sclerosis and CFS (8, 53, 54, 55). Examples of psychologisation include
the citation of higher estimates in support of a 'psychosomatic' explanation,
and not documenting, or unfairly dismissing lower rates. In other cases, authors
may deliberately overlook the flaws associated with a particular measure,
leading them to exaggerate the significance of psychiatric illness associated
with a disease.

For
instance, it is well known that estimates may be inflated as a result of
confounding, i.e. the inclusion of symptoms of the medical condition as criteria
for the diagnosis of psychiatric disorders (56, 57, 58, 59). The symptoms most
often used for this purpose include fatigue, insomnia, loss of appetite,
psychomotor retardation and difficulties with concentration (60, 61, 62, 63, 64,
65). Not surprisingly, omitting one or more of these from the list of criteria
can have a significant effect on the estimates of psychopathology. For example,
in their study on chronic fatigue, Katon et al eliminated fatigue as a criterium
of depression and found that this alone reduced the prevalence rate from 15.3%
to 10.2% (66).

The
inclusion of disability-related items in self-rating scales can cause similar
problems. For instance, Yeomans and Conway (53) reported that 33% of their
patients with ME scored 11 or more on the depression subscale of the Hospital
Anxiety and Depression questionnaire (HAD). However, when they excluded the item
'I feel as if I am slowed down', no one exceeded the cut-off point for caseness.

The
reliance on symptoms can also lead to false positives in relation to
somatisation disorder (SD). For instance, estimates of SD in patients with CFS
have varied from 0% to 98% (67). When one team of researchers excluded 7 somatic
items from the diagnostic criteria, this reduced the prevalence rate from 46% to
20% (66). Reduced rates have also been noted by others, leading Johnson et al
(67) to conclude that the "diagnosis of SD is of limited use in populations
in which the aetiology of the illness has not been established."

In
order to assess whether the psychological disturbances reported by people with
CFS represent a reaction to their illness or the presence of a primary
psychiatric condition, researchers have compared this population with people
suffering from multiple sclerosis (68, 69), rheumatoid arthritis (66), cystic
fibrosis (70), spinal cord injuries (8) and muscle disorders (71, 72).
Unfortunately, it is difficult to interpret most of these studies because they
failed to match the samples with regard to the degree of impairment or the
severity of symptoms. In relation to fatigue, the levels recorded by the
comparison groups were often significantly lower than those of the patients with
CFS. Where fatigue was not assessed, other illness-related variables showed that
the controls had fewer symptoms than the people with chronic fatigue (66).

Despite
the flaws, most reviewers have concluded that patients with CFS have higher
rates of psychiatric disorders than other disabled groups. However, the failure
to control for the degree of impairment means that their emphasis on
psychopathology as a major factor in the perpetuation of CFS is probably not
justified (73, 74, 75).

6.
Psychologisation and the illusion of control.

While
psychologisation can have serious and occasionally fatal consequences (40, 76,
77), it also offers certain advantages (78, 79). For instance, Taylor (79) found
that many women with breast cancer believed that stress management techniques
and a positive attitude would prevent a recurrence. Although there is little
research evidence which supports this view (80, 81), both she and Turnquist et
al (82) consider these 'illusions' to be adaptive, enabling more women to cope
with the fear, vulnerability and helplessness associated with their illness.

The
reverse is true when outsiders claim that patients create and are responsible
for their symptoms (6, 10). A discussion of victim-blaming statements can be
found in texts by Sontag (83) and Wilkinson and Kitzinger (84). For instance,
Sontag documents how cancer patients were once described as having a "great
tendency for self-pity" and as being "empty of feeling and devoid of
self". In more general terms, it was alleged that the "sick man
himself creates his disease" and that "illness is in part what the
world has done to a victim, but in a larger part it is what the victim has done
with his world, and with himself."

In
her response, Sontag concludes that "such preposterous and dangerous views
manage to put the onus of the disease on the patient... The view of cancer as a
disease of the failure of expressiveness condemns the cancer patient; expresses
pity but also conveys contempt." To that might be added that the emphasis
on the spiritual flaws of the sick and disabled will make many patients feel
guilty, thus further increasing their distress.

So
who gains from this approach? Outsiders might be tempted to play down the
influence of factors such as viruses and pollution - over which mankind has
relatively little control - to enhance their 'sense of mastery' over their lives
(79). By attributing them to personal flaws (which one doesn't share), one
reduces one's own perceived risk of being struck down by a feared disease.

A
variation on this theme is the suggestion by Lerner and Simmons (78) that
'blaming the victim' helps people to maintain their belief in a 'just world',
where people get what they deserve and deserve what they get. According to this
hypothesis, individuals can avoid adversity through their own activities but
this also implies that those struck by misfortune are deemed to have somehow
merited their fate.

Surprisingly,
such a view of illness is not restricted to a small group of 'New Age'
philosophers or the odd clinical text (6). Wortman and Dunkel-Schetter (85)
wrote that health care professionals "often have ambivalent feelings
towards their patients - patients they are supposedly trying to help. Past
research has suggested that even a single encounter with a victim can be a
powerfully distressing experience, and can result in blame and derogation of the
victim." Thus the occasional comment which insinuates that the patient's
character made them ill may be part of a coping strategy which allows
practitioners to protect themselves from unpleasant emotions, even though it
will almost certainly undermine the relationship with those in their care.

Finally,
blaming the victim may result from strongly held political views (84). For
instance, some believe that health is a matter of personal responsibility and
that people increase their risk of disease by engaging in behaviours like
smoking or eating an unhealthy diet. The politically motivated may exaggerate
the influence of lifestyle or apply this reasoning to other conditions, to limit
funds destined for research and restrict patients' eligibility for certain
benefits. Thus they will argue that if the cause of illness lies in people's
character and behaviours, then fewer resources have to be spent evaluating the
effects of environmental pollutants, pesticides and other external factors
implicated in disease. Unless governments redirect the savings to educational
projects concerned with prevention, or to support those already affected,
blaming the victim is a useful way of freeing-up funds and diverting resources.

Psychologisation
of food allergy and intolerance.

Examples
of psychologisation can also be found in the literature on food sensitivities.
Most of these focus on the apparently high prevalence of psychiatric disorders
in this population, with the implication that these are the main source of the
patients' complaints (86). However, as will be argued in the following section,
such suggestions should be interpreted with care.

A
major difficulty in assessing the actual role of psychological factors in food
allergy and intolerance is that the majority of the studies have included
patients with multiple chemical sensitivities and 'environmental illness' (87,
88). To complicate matters, some of the subjects were engaged in legal action
for compensation at the time (89), and many had supposed rather than proven
allergies (90). Indeed, few studies have restricted participation to patients
with properly diagnosed food sensitivities and even fewer have assessed delayed
reactions to food, presenting 24 hours or more after ingestion.

Another
problem is the assessment of psychiatric morbidity and the use of measures which
include the symptoms of food sensitivity as criteria of psychopathology. As
noted above, such confounding can lead to diagnostic false positives (87, 88)
and give a misleading view of these patients' mental health.

This
is certainly the case in relation to somatisation disorder, where the criteria
in DSM-IV require the presence of seven symptoms from a list which includes
nausea, bloating and intolerance to several different foods, as well as headache
and abdominal pain (56). Accordingly, it is advisable to obtain additional
evidence such as the presence of conflicts and other stressors at meal times or
obvious signs of secondary gain, before attributing these symptoms to SD. If the
aetiology is unclear, it may also be useful to engage the patient in an
experiment, for instance, to compare the effects of standard treatments such as
avoidance with the results of psychotropic medication (91). A positive response
to the latter does not prove that the reaction to food was mediated by emotional
as opposed to immunological factors, but it could give useful insights into the
mechanisms underlying specific symptoms, and clarify the role of contributory
factors.

Some
clinicians consider the documented rates of psychopathology to be reliable,
arguing that symptoms such as depression are generally not triggered by food
(90). However, others remain unsure and have pointed to evidence linking diet
with a number of psychological disturbances, including affective disorders and
schizophrenia (7, 92, 93, 94).

As
noted above, the finding of high rates of psychopathology does not prove that
those disorders caused the patients' symptoms. Depression and anxiety may be
due, at least in part, to factors such as uncertainty. In previous research,
uncertainty relating to conditions like myocardial infarction, multiple
sclerosis and CFS was significantly correlated with psychological distress (8,
95, 96). It is therefore possible that this variable also plays a role in people
with food allergies and sensitivities. Similarly, any mood disturbances may be
exacerbated and perpetuated as a result of continued psychologisation by
physicians and family (41, 97, 98). These are just two of the factors which
should be considered when assessing the psychological status of individuals with
food sensitivities (8). Focusing exclusively on the prevalence of affective
disorders could lead to mistakes.

In
differentiating cause and effect, a prior history of psychiatric illness is
often regarded as suggestive of a psychological vulnerability (99). The problem
here is obvious. Without corroboration from accurate medical notes, much depends
on the patient's memory and their own interpretation of their complaints (88).
Moreover, if one has to rely on the patient, it must be remembered that current
psychological distress can increase the tendency to recall some symptoms and
health events at the expense of others. Moreover, it is possible that past
symptoms were the result of conditions like malabsorption and altered gut
ecology, which might have predisposed patients to develop sensitivities to food
later in life (100). Leaving these considerations aside, there is at present
little evidence that people with proven food reactions are more likely to have a
history of psychiatric morbidity or that they have a greater psychological
vulnerability than people who do not experience reactions to foods (101).

Finally,
it has been suggested that blaming symptoms on allergies and environmental
toxins may help people with psychiatric disorders to avoid the stigma of mental
illness (24, 86). In a society where the general population and certain
physicians still regard psychiatric disorders as less worthy of attention and
respect than physical ones, it is understandable that some patients might choose
to blame their unexplained symptoms on allergies rather than depression or
anxiety. One can also postulate that these erroneous attributions may be
reinforced by some self-help groups and articles in the popular press (102).
However, there is still no convincing evidence that most patients with food
allergies are motivated by prejudiced views of mental illness. Moreover, until
every patient is also assessed for conditions like dysbiosis and tested for
immune activation (103), one cannot assume that their attributions are
incorrect.

In
summary, most of the claims that psychological factors are the source of food
sensitivities seem to be based on methodologically flawed research and a biased
interpretation of the findings. Moreover, the lack of studies on well-defined
groups means that writers have tended to generalise from one population to
another, which may not be justified. In this respect, it is worth noting the
findings of Peveler et al (101). They assessed patients from the community and
found that individuals who attributed their symptoms to food sensitivity
suffered less psychological impairment than those who attributed their
complaints to stomach or bowel disorders and stress. The estimated rate of
psychiatric illness was also relatively low, and they noted a strong
relationship between the patients' attribution of symptoms to foods and the
clinical judgement of food sensitivity. These findings show that the research
relating to allergy clinic patients and people with alleged allergies or various
environmental syndromes cannot be generalized to people with food intolerance
from the general population. They also suggest that many patients' beliefs about
food sensitivity are probably accurate and that claims of widespread
misattribution were premature.

Solutions.

Perhaps
the most important and effective remedy for psychologisation in the clinic is
for scientists to stop using psychological explanations as a convenient
'dust-bin' for complex cases or troublesome patients. In this hi‑tech age,
where doctors depend more and more on the results from laboratory tests and
objective clinical signs, a psychological diagnosis can explain the otherwise
inexplicable. It is often plausible, difficult to disprove and can be altered to
suit changing circumstances. To put it another way, a psychological explanation
may be an attractive option for practitioners who lack financial resources
and/or time. However, as many writers have pointed out (e.g. 104), it might
serve health care professionals better to be 'agnostic' every now and then.

As
for the examples in the literature, a more objective and critical approach by
reviewers and editors should help to avoid most cases of bias. For instance,
McEvedy and Beard's assessment of the outbreak at the Royal Free Hospital was
largely based on information from selected case-notes and a highly subjective
evaluation of the evidence (9). Their misrepresentation of the data constituted
a clear case of psychologisation, reflecting not only their own lack of respect
for science but also the editors' failure to address the paper's many flaws.

The
same lack of editorial interest in accuracy and balance has allowed more recent
articles to exaggerate the role of psychiatric morbidity in CFS (75, 105, 106).
Here writers rarely consider alternative explanations for the associated mood
disorders, such as the effect of uncertainty, the strain of the illness and the
lack of social support (8, 24). This bias illustrates the editors' continued
preference for simple, psychological explanations at a time when the evidence
points to a heterogeneous population and a multifactorial aetiology (107, 108,
109, 110). In fact, the predilection for simplistic theories and lack of
interest in alternative views features in many cases of psychologisation, not
just those related to CFS.

People
are entitled to their opinion and I am not suggesting that speculation has no
place in scientific texts. However, unsubstantiated or poorly supported claims
should be acknowledged as such and interpreted with care. In this age of
evidence-based medicine, writers must consider all reasonable explanations, and
take account of methodological flaws and valid criticisms.

It
is my belief that articles with a strong bias towards one explanation and
an unbalanced or unfair approach to the available data, do not belong in
scientific publications unless marked as an opinion piece. Respect for plausible
alternative views and the evaluation of all the relevant evidence are not
luxuries, to be indulged in should space permit. A broader editorial policy may
produce more readable and provocative articles but it also leads to
psychologisation and accordingly, to misunderstanding, inappropriate advice and
much needless distress.

Footnote

1.
It is generally accepted that CFS is not a single entity, but that the term
covers a number of disorders, all characterised by unexplained fatigue. The
evidence supports the view that ME should be regarded as a subgroup of CFS.

REFERENCES

1
Goudsmit EM and Gadd R. All in the mind? The psychologisation of illness. The
Psychologist 1991; 4: 449-453.

2
Rippere V. The mental state of dismissed patients - an enquiry into dismissal
injury. V. Repercussions of psychogenic dismissal. Newsletter of the Society for
Environmental Therapies 1992; 12: 138-148.